Neuroprotective Effects of Flaxseed and Purslane Extracts against Cerebral Ischemia/Reperfusion Injury: Modulation of Apoptotic, Neurotrophic, and Neurotransmitter Signaling

Authors

• Fatma M. Attia, Zoology and Entomology Department, Faculty of Science, Capital University, Cairo, Egypt
• Ahmed E. Abdel Moneim, Zoology and Entomology Department, Faculty of Science, Capital University, Cairo, Egypt
• Rehab E. El-Hennamy, Zoology and Entomology Department, Faculty of Science, Capital University, Cairo, EgyptFollow
• Inas S. M. Elsayed, Physiology Department, Egyptian Drug Authority, Giza, Egypt
• Gehad E. Elshopakey, Department of Clinical Pathology, Faculty of Veterinary Medicine, Mansoura University, Mansoura 35516, Egypt.
• Nabil A. El-Yamany, Zoology and Entomology Department, Faculty of Science, Capital University, Cairo, Egypt

Document Type

Original Study

Keywords

Cerebral ischemia/reperfusion; Flaxseed/Purslane extracts; Apoptosis; BDNF; Neural amino acids; Monoamine neurotransmitters.

Abstract

Background: Cerebral ischemia/reperfusion (I/R) injury is a serious pathological condition that leads to permanent neurological impairment. Plant-derived bioactive compounds are gaining attention as promising neuroprotective therapeutic alternatives with relatively low adverse effects. Aims: This study aimed to investigate the neuroprotective effects of flaxseed extract (FE) and purslane extract (PE) on I/R injury in rats.

Methods: Seventy adult male rats were divided into seven groups: control, sham, I/R model, FE, FE-pretreated I/R, PE, and PE-pretreated I/R. Cerebral ischemia was induced by occlusion of the bilateral common carotid arteries for 60 min, followed by 120 min reperfusion. Rats were treated orally with FE or PE (200 mg/kg) for 14 days before the induction of ischemia.

Results: Biochemical studies demonstrated that cerebral I/R significantly upregulated apoptotic signaling, with increased levels of caspase-3 (125.92%) and Bcl-2-associated X protein (66.66%), and decreased levels of B cell lymphoma-2 (−44.28%) and brain-derived neurotrophic factor (−52.73%). In addition, ischemic insult induced pathophysiological changes in sodium/potassium ATPase (−58.33%), acetylcholinesterase (64.91%), dopamine (−50.90%), norepinephrine (−37.31%), serotonin (−49.91%), glutamate (94.93%), and aspartate (97.87%). Conversely, significant decreases in the inhibitory neurotransmitters gamma-aminobutyric acid (−40.35%) and glycine (−61.98%) were observed following I/R injury. Pretreatment with FE or PE before ischemic induction effectively attenuated these changes by suppressing apoptotic pathways, as evidenced by decreases in Bcl-2-associated X protein (FE: −20.55%; PE: −28.88%) and caspase-3 (FE: −31.14%; PE: −40.98%), and increases in B cell lymphoma-2 (FE: 29.48%; PE: 39.74%) and brain-derived neurotrophic factor levels (FE: 75.63%; PE: 89.49%). Pretreatment also improved neurotransmitter homeostasis, including dopamine (FE: 17.95%; PE: 41.13%) and aspartate (FE: −16.12%; PE: −22.58%), and restored neuronal enzyme function.

Conclusions: These findings indicate that FE and PEs exert significant neuroprotective effects against cerebral I/R injury, which might be attributed to the modulation of apoptosis and neurotransmitter regulation. Notably, PE exerted relatively greater neuroprotective efficacy, particularly in modulating apoptotic markers and restoring neurotransmitter homeostasis.

How to Cite This Article

Attia, Fatma M.; Abdel Moneim, Ahmed E.; El-Hennamy, Rehab E.; Elsayed, Inas S. M.; Elshopakey, Gehad E.; and El-Yamany, Nabil A. (2026) "Neuroprotective Effects of Flaxseed and Purslane Extracts against Cerebral Ischemia/Reperfusion Injury: Modulation of Apoptotic, Neurotrophic, and Neurotransmitter Signaling," Trends in advanced sciences and technology: Vol. 3, Article 14.
DOI: 10.62537/2974-444X.1063
Available at: https://tast.researchcommons.org/journal/vol3/iss1/14